Pancreatic cancer (PC) is the most lethal tumor type among human diseases, with low survival rate. The investigation of potent molecular mechanisms involved in PC is still obscure owing to its drug resistance. The purpose of this study is to disclose the underlying mechanism participating in PC progression and drug therapy, reversing the unpromising treatment outcome. In our research, miR-760 was firstly revealed to be lowly expressed in PC cells. And upregulation of miR-760 could further suppress PC cell proliferation and boost cell apoptosis, as well as improve gemcitabine sensitivity of PC cells through gain-of-function assays. Besides, RNA-binding protein (RBP) MOV10 interacted with and stabilized Integrin β1 (ITGB1). Furtherly, miR-760 was proved to target MOV10 mRNA to decrease MOV10 protein expression, thus promoting the destabilization of ITGB1. At last, rescue experiments validated that upregulation of ITGB1 remedied the miR-760 overexpression-caused inhibition on biological activities and gemcitabine resistance of PC cells. To summarize, the current inspection demonstrated that miR-760 enhances sensitivity of PC cells to gemcitabine through modulating MOV10-stablized Integrin β1, highlighting the role of miR-760/MOV10/ITGB1 pathway in the drug therapy for PC patients.

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